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IPFC 2 Midterm 2 > Pathophysiology of Dyspepsia, GERD, and PUD > Flashcards

Pathophysiology of Dyspepsia, GERD, and PUD Flashcards

1
Q

What is the requirement to have dyspepsia as a symptom? (2)

A
  • Last one month
  • epigastric pain is dominant
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2
Q

What are other symptoms people with dyspepsia can have? (4)

A
  • N/V
  • burping/bloating
  • Early satiety (getting full quickly)
  • Heartburn
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3
Q

When do we refer patients?

A

alarm VBAD symptoms
- Vomiting 7+ days
- Bleeding (vomitting blood, coffee ground (old blood), dark tarry stools
- Anemia/Anoerixa/Abdominal mass (unexplained symptoms of dizziness, weight loss, cold)
- Dysphagia (difficulty, pain swallowing)

OR

Any patient OVER 60 with new or worsening symptoms
- severity of symptoms does not equal severe condition

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4
Q

What do patients with dyspepsia who do not require referral considered?

A

Considered UNINVESTIGATED dyspepsia

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5
Q

Anatomy of the Lower esophageal sphincter
Internal and External

A

Internal: thickened smooth muscle of distal esophagus
- strengthens it

External: Crural (leg) part of diaphragm
- Applies pressure to internal LES

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6
Q

Anatomy of Squamocolumnar junction? (2)

A

Esophageal mucosa: strat squamous
Gastric mucosa: columnar cells + protective mucous layer

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7
Q

What is the function of the LE sphincter? What is its state at rest vs when swallowing?

A

Function
- prevents backflow of stomach contents (acidic, pepsin) into esophagus

At rest = contracted, closed
When swallowing = relaxed, open

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8
Q

Why is some degree of reflux normal especially after meals? What protects it? (2)

A
  • saliva neutralizes acidic gastric content
  • secondary peristaltic waves help return reflux into stomach
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9
Q

What is the most common reason of GERD? What are 2 less significant reasons?
What is NOT a reason of GERD

A

Most common
- increased transient LES relaxation

Less significant
- Decreased LES tone at rest
- Delayed gastric emptying

NOT a reason
- due to increased gastric acid secretion

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10
Q

What are non-modifiable GERD risk factors?

A
  • Age
  • Pregnancy
  • Family history
  • Scleroderma
  • Zollinger-ellison syndrome (excessive acid production even if LES tone is good)
  • Hiatal hernia (inc intraabdominal pressure)
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11
Q

Explain Hiatal hernia. What is it associated with (2) What are 3 risk factors of it (3)

A

Lower part of esophagus and upper part of stomach push through diaphragm and into chest cavity (changes angle)

Associated with
- loss of external LES support
- changes angle of His

Risk factors
- 50+ years
- Obesity
- smoking

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12
Q

What are modifiable GERD risk factors? (8)

A
  • Obesity
  • Smoking (lowers LES pressure, low saliva)
  • Medications
  • Eating fatty/fried foods (delays gastric emptying)
  • Drinking alcohol (lowers LES pressure)
  • Eating chocolate/peppermint (lowers LES pressure)
  • Delayed gastric emptying/large meals (inc LES pressure/large volume for reflux)
  • Sleeping
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13
Q

What medications are risk factors (6)

A
  • anticholinergics
  • benzodiazepines
  • calcium channel blockers
  • nitrate
  • opioids
  • tricyclic antidepressants
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14
Q

What are complications of GERD? (3)

A
  1. Erosive esophagitis EE
    - inflammation of squamous epithelium causing erosion of esophageal mucosa + decreased peristalsis
  2. Esophageal stricture
    - Scar tissue replaces erosive esophagitis causing a narrow esophagus
  3. Barrett’s Esophagus
    - esophageal epithelium becomes replaced with columnar cells
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15
Q

What are things that can worsen GERD?

A
  • Spicy or acidic foods
    Meds:
  • Bisphosphonates
  • Aspirin and NSAIDs
  • Potassium and iron salts
  • Tetracycline, doxycycline, clindamycin
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16
Q

How to diagnose GERD?

A
  1. Classic symptoms that are mod-severe (impact daily activities) OR occur 2+ times/week

OR

  1. Evidence of complications, regardless of symptoms
17
Q

When do we use additional investigations such as endoscopy? (2)

A
  • When VBAD alarm symptoms are present
  • If not responding to therapy
18
Q

Why are infants more susceptible to GER? (3) is it normal?

A
  • Blunted angle of His
  • LES not fully matured
  • Frequently laying down

Normal
- peaks around 4 months, resolves in 1 year

19
Q

What are the gastric cell types from outside (laminal) to inside (basal) (5)

A
  1. Surface mucous cells
    - secrete mucous and bicarb
  2. Parietal cells
    - secrete H+ and Cl- and produce intrinsic factor
  3. Neck mucous cells
    - secrete mucous and bicarb to prevent pepsinogen from eating the stomach
  4. Chief cells
    - secrete pepsinogen and lipase
  5. Enteroendocrine cells
20
Q

What do enteroendocrine cells secrete? (3)

A
  1. Enterochromaffin-like cells
    - Produce histamine -> stimulates ONLY parietal cells (HCl)
  2. G-cells
    - Produce gastrin -> stimulation parietal (HCl) + chief cells (pepsin) (and peristalsis)
  3. D-cells (stimulated by acid presence)
    - produces somatostatin –> inhibit G-cells (gastrin), parietal cells (HCl), and enterochromaffin cells (histamine)
    - negative feedback loop for HCl production
21
Q

Where do PPIs and H2RAs act?

A

PPIs
- inhibit parietal cell action (to stop HCl production)
- lumen side

H2RA
- act in enterochromaffin-like cells to block histamine from binding to parietal cells
- non-lumen side

22
Q

What is Peptic ulcer disease?

A

Gastric juices overwhelms defensive properties of mucous

23
Q

What are the main 2 causes of PUD? What are other causes?

A

1) NSAID use
- 4x increase risk of gastric ulcers

2) H. pylori infection
- 6-10x increase in risk of PUD

Other
- Zollinger- ellison syndrome (excessive acid)
- Other meds alongisde NSAIDs
eg. tylenol 2+g/day, bisphosphonates, prednisone, clopidogrel, spironolactone, SSRI, anticoagulants

24
Q

Explain pathophysiology of NSAID induced ulcer (2)

A

Systemic effects
- COX-1 enzyme produced prostaglandins that are gastroprotective (NSAIDs block this)

Local effects
- When the drug gets ionized in neutrol environment after passing mucosa –> cause local toxicity

25
Q

What is the highest risk NSAID and lowest risk NSAID?

A

Highest risk: ketorolac
Lowest risk: COX-2 selective agents (celecoxib)

26
Q

What do PUD symptoms look like?

A

Usually no symptoms until complications develop
- Complications like anemia, coffee-ground emesis, black stools

When present
- it can go away and come back
- Similar to dyspepsia

27
Q

What does the diagnosis of PUD require?

A

Requires ulcer visualization

OR

non-invasive H. pylori testing is recommended for patients under 60 years

28
Q

How is h. pylori acquired? What does it do?

A

Acquired through fecal-oral route in childhood
- Neutralizes the acid around it to grow, then produces enzymes to break down the mucosa

IPFC 2 Midterm 2 (5 decks)

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